Allergic conjunctivitis, like other allergic diseases, is thought to be mediated by CD4+ T lymphocytes producing the TH2-associated cytokines, Interleukin-4 (IL-4) and IL5. Since allergic disease is clearly a TH2-mediated phenomenon, previous studies in our laboratory have focused on factors which drive TH2 specific cytokine expression. A factor which we believe is required for IL-4 gene expression in human and mouse T cells is the transcription factor CP2. To understand how the CP2 factor participates in IL-4 gene expression and the etiology of allergic disease, we propose to remove or "knockout" the CP2 gene in mice via homologous recombination, and then use the CP2-deficient mice in our experimental model of allergic conjunctivitis. We anticipate that if CP2 is important for TH2 production, our CP2 "knockout" mice will be resistant to allergic conjunctivitis. Knowledge gained from these studies will be important in delineating the role of CP2 in gene regulation, such information may lead to the development of novel therapies for allergic disease.